ArticleProceedings of the National Academy of Sciences of the United States of America1995
Serine-1321-independent regulation of the mu 1 adult skeletal muscle Na+ channel by protein kinase C.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 66 citations in OpenAlex.
- Characterization of a new sodium channel mutation at arginine 1448 associated with moderate Paramyotonia congenita in humans.The Journal of physiology · 1999Trial
- Nernst-Planck-Gaussian finite element modelling of CaFrontiers in physiology · 2024Article
- Exercise and fatigue: integrating the role of KEuropean journal of applied physiology · 2023Review
- Closed-state inactivation of cardiac, skeletal, and neuronal sodium channels is isoform specific.The Journal of general physiology · 2022Article
- Finite element analysis predicts CaScientific reports · 2021Article
- Review
- Sarcoplasmic reticular CaScientific reports · 2021Article
- CaMKII enhances voltage-gated sodium channel Nav1.6 activity and neuronal excitability.The Journal of biological chemistry · 2020Article
- Sodium current inhibition following stimulation of exchange protein directly activated by cyclic-3',5'-adenosine monophosphate (Epac) in murine skeletal muscle.Scientific reports · 2019Article
- The Sick and the Weak: Neuropathies/Myopathies in the Critically Ill.Physiological reviews · 2015Review
- On the multiple roles of the voltage gated sodium channel β1 subunit in genetic diseases.Frontiers in pharmacology · 2015Review
- Post-translational modifications of voltage-gated sodium channels in chronic pain syndromes.Frontiers in pharmacology · 2015Review
- Protein kinase C enhances human sodium channel hNav1.7 resurgent currents via a serine residue in the domain III-IV linker.FEBS letters · 2014Article
- Regulation of sodium channel activity by phosphorylation.Seminars in cell & developmental biology · 2011Review
- Role of Ca(2+) in injury-induced changes in sodium current in rat skeletal muscle.American journal of physiology. Cell physiology · 2009Article
- Beta1-subunit modulates the Nav1.4 sodium channel by changing the surface charge.Experimental brain research · 2006Article
- Dysregulation of sodium channel gating in critical illness myopathy.Journal of muscle research and cell motility · 2006Review
- Rapid protein kinase C-dependent reduction of rat skeletal muscle voltage-gated sodium channels by ciliary neurotrophic factor.The Journal of physiology · 2005Article
- Regulation of sodium channel function by bilayer elasticity: the importance of hydrophobic coupling. Effects of Micelle-forming amphiphiles and cholesterol.The Journal of general physiology · 2004Article
- Channel activation voltage alone is directly altered in an isoform-specific manner by Na(v1.4) and Na(v1.5) cytoplasmic linkers.The Journal of membrane biology · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The adult skeletal muscle Na+ channel mu1 possesses a highly conserved segment between subunit domains III and IV containing a consensus protein kinase C (PKC) phosphorylation site that, in the neuronal isoform, acts as a master control for "convergent" regulation by PKC and cAMP-dependent protein kinase. It lacks an approximately 200-aa segment between domains I and II though to modulate channel gating. We here demonstrate that mu1 is regulated by PKC (but not cAMP-dependent protein kinase) in a manner distinct from that observed for the neuronal isoforms, suggesting that under the same conditions muscle excitation could be uncoupled from motor neuron input. Maximal phosphorylation by PKC, in the presence of phosphatase inhibitors, reduced peak Na+ currents by approximately 90% by decreasing the maximal conductance, caused a -15 mV shift in the midpoint of steady-state inactivation, and caused a slight speeding of inactivation. Surprisingly, these effects were not affected by mutation of the conserved serine (serine-1321) in the interdomain III-IV loop. the pattern of current suppression and gating modification by PKC resembles the response of muscle Na+ channels to inhibitory factors present in the serum and cerebrospinal fluid of patients with Guillain-Barré syndrome, multiple sclerosis, and idiopathic demyelinating polyradiculoneuritis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.